Gallic acid / ROS Cancer Research Results

GA, Gallic acid: Click to Expand ⟱

Features:

Phenolic acid found in gallnuts, sumac, witch hazel, tea leaves, oak bark. Has antioxidant, antimicrobial and anti-obesity properties.
The GA derivatives include two types: ester and catechin derivatives. The most common ester derivatives of GA are alkyl esters, which are composed mainly of methyl gallate (MG), propyl gallate (PG), octyl gallate (OG), dodecyl gallate (DG), tetradecyl gallate (TG), and hexadecyl gallate (HG), and some of the main catechin derivatives are epicatechin (EC), epicatechin gallate (ECG), epigallocatechin (EGC), gallocatechin gallate (GCG), and epigallocatechin gallate (EGCG)

Gallic acid is a naturally occurring polyphenol found in a variety of plant-based foods. Some of the best dietary sources include:

Fruits:
Berries (strawberries, blackberries, blueberries)
Grapes, including red wine (grapes are rich in polyphenols)
Pomegranates and apples
Nuts and Seeds: Walnuts and almonds have been noted to contain GA in their skins
Herbs and Spices: Tea (especially green tea), Sumac and other spices
Other Plants: Gallnuts (from oak trees)

Pathways:
-ROS generation in tumor cells is frequently reported, Antioxidant behavior dominates in normal tissue models -Apoptosis Induction: Activating caspase cascades, Shifting Bax versus Bcl-2, MMP, cyt-c release -Cell Cycle Arrest: typ @ G1 or G2/M checkpoints.
-Anti-inflammatory Effects: inhibiting NF-κB
-reported Angiogenesis Inhibition:
-Modulation of Signaling Pathways: MAPK Pathway, PI3K/Akt Pathway Inhibition, p53 Pathway

Gallic acid exhibits a complex behavior with ROS in cancer cells, acting as both an antioxidant and a pro-oxidant depending on the context and its concentration:

Antioxidant Effects at Low Doses:
-At lower concentrations, gallic acid is typically characterized by its ability to scavenge free radicals, thus reducing oxidative stress.
This antioxidant property may help protect normal cells from DNA damage, reducing the risk of mutations that could lead to cancer.

Pro-oxidant Effects at High Doses: >50-100uM?
-Capable of biphasic redox behavior (antioxidant in normal cells, pro-oxidant in some tumor contexts) -At higher concentrations, GA can exert pro-oxidant effects, generating ROS within cancer cells. Elevated ROS levels can overwhelm the cellular antioxidant defenses of cancer cells, leading to oxidative stress, mitochondrial dysfunction, and ultimately cell death.

Oral bioavailability is well absorbed but subject to rapid conjugation (glucuronide/sulfate/methylated metabolites). Many cytotoxic in-vitro concentrations are in the 10–100 µM range, often higher than typical plasma levels after dietary intake.

Gallic acid — Gallic acid is a naturally occurring trihydroxybenzoic phenolic acid and plant secondary metabolite with antioxidant, pro-oxidant, anti-inflammatory, antimicrobial, and extensively studied preclinical anticancer activity. It is formally classified as a low-molecular-weight polyphenolic phenolic acid and is commonly abbreviated GA. Its chemical identity is 3,4,5-trihydroxybenzoic acid. Dietary and botanical sources include gallnuts, sumac, tea, grapes, berries, pomegranate, mango, walnuts, oak bark, and hydrolysable tannins. GA is also released during digestion or microbial metabolism of gallotannins and galloylated polyphenols. Its anticancer effects are strongly concentration-, cell-type-, redox-, and exposure-dependent.

Primary mechanisms (ranked):

Biphasic redox modulation, with ROS generation and oxidative stress predominating in susceptible cancer cells at cytotoxic concentrations, but ROS scavenging and NRF2-linked antioxidant protection predominating in many normal or inflamed tissues.
Mitochondrial apoptosis through mitochondrial membrane depolarization, Bax/Bcl-2 imbalance, cytochrome-c release, caspase activation, and PARP cleavage.
Suppression of oncogenic survival signaling, particularly PI3K/AKT, STAT3, EGFR, and context-dependent MAPK signaling.
Cell-cycle arrest through modulation of p53, p21, p27, cyclins, and cyclin-dependent kinases, commonly at G1 or G2/M depending on the model.
Suppression of inflammatory and tumor-promoting transcription through NF-κB inhibition and reduced COX-2, IL-6, TNF-α, and related mediators.
Inhibition of angiogenesis through PTEN/AKT/HIF-1α/VEGF signaling and reduced endothelial or tumor-associated vascular responses.
Suppression of invasion, migration, epithelial-mesenchymal transition, and matrix-remodelling pathways, including MMP2, MMP9, Wnt/β-catenin, and selected EMT regulators.
Metabolic disruption through context-dependent inhibition of glycolysis, LDH-associated lactate metabolism, lipid synthesis, and other tumor bioenergetic processes.
Therapy sensitization reported with selected cytotoxic and targeted agents, including paclitaxel, carboplatin, camptothecin, and olaparib, but currently supported mainly by cell-culture evidence.

Bioavailability / PK relevance: GA can be absorbed orally and is among the more readily absorbed simple polyphenols, but absorption is followed by rapid methylation, glucuronidation, sulfation, microbial transformation, and urinary elimination. Circulating exposure consists substantially of conjugated and microbial metabolites rather than persistent free GA. Formulation strategies such as nanoparticles, conjugates, and encapsulation can increase exposure experimentally, but these delivery systems remain investigational.

In-vitro vs systemic exposure relevance: Many anticancer experiments use approximately 10–100 µM GA, with pronounced pro-oxidant cytotoxicity frequently occurring toward the upper portion of this range or above it. These free-compound concentrations commonly exceed sustained plasma concentrations expected from ordinary dietary intake. Consequently, direct systemic anticancer effects demonstrated at high micromolar exposure may not be achievable through food consumption or conventional oral supplementation. Local gastrointestinal exposure, metabolites, tissue accumulation, or engineered delivery could produce different exposure relationships.

Clinical evidence status: Preclinical. GA has extensive cell-culture evidence and a smaller body of animal evidence across multiple tumor types. Human pharmacokinetic and food-intervention studies confirm exposure to GA and its metabolites, but isolated GA has not established anticancer efficacy in randomized clinical trials and is not an approved cancer therapy. Human studies involving polyphenol-rich mango, pomegranate, tea, grape, or botanical preparations cannot be attributed specifically to GA. Therapy-sensitizing activity remains experimental and should not be used to justify combining GA supplements with chemotherapy outside clinical supervision.

Gallic Acid Mechanistic Profile

Rank	Pathway / Axis	Cancer Cells	Normal Cells	TSF	Primary Effect	Notes / Interpretation
1	Biphasic redox modulation	ROS ↑; oxidative stress ↑ (dose-dependent) (model-dependent)	ROS ↓; radical scavenging ↑; antioxidant capacity ↑	P, R	Selective redox destabilization	Pro-oxidant tumor effects are most evident at higher in-vitro concentrations; antioxidant effects dominate in many non-malignant injury models.
2	Mitochondrial apoptosis	Mitochondrial membrane potential ↓; Bax ↑; Bcl-2 ↓; cytochrome-c ↑; caspases ↑; PARP cleavage ↑	↔ or apoptosis ↓ under oxidative injury (context-dependent)	R, G	Intrinsic apoptotic cell death	Frequently downstream of ROS accumulation, although mitochondrial and apoptotic responses vary by tumor genotype and concentration.
3	PI3K AKT survival signaling	PI3K ↓; p-AKT ↓; mTOR signaling ↓ (model-dependent); PTEN ↑	↔ or AKT-associated cytoprotection ↑ during inflammatory injury	R, G	Growth and survival suppression	Direction can differ between malignant cells and stressed normal tissues; pathway effects should be entered with context qualifiers.
4	Cell-cycle checkpoints	p53 ↑; p21 ↑; p27 ↑; cyclin D1 ↓; cyclin E ↓; G1 or G2/M arrest ↑	↔	G	Cytostasis	Arrest phase is model-dependent and should not be generalized to one checkpoint.
5	NF-κB inflammatory signaling	NF-κB ↓; COX-2 ↓; IL-6 ↓; TNF-α ↓; pro-survival inflammation ↓	NF-κB ↓; inflammatory cytokines ↓; epithelial protection ↑	R, G	Anti-inflammatory and anti-survival signaling	One of the more reproducible effects across tumor and non-tumor inflammatory models.
6	MAPK stress signaling	JNK ↑; p38 ↑; ERK ↓ or ↔ (context-dependent)	Pathologic p38 and ERK activation ↓ or protective signaling ↑ (context-dependent)	P, R	Stress-response reprogramming	MAPK direction depends on cell type, initiating stress, exposure duration, and whether apoptosis or cytoprotection is being measured.
7	Angiogenesis and hypoxia signaling	PTEN ↑; AKT ↓; HIF-1α ↓; VEGF ↓; angiogenesis ↓	↔	G	Anti-angiogenic activity	Supported by selected ovarian, cervical, and other experimental cancer models; not clinically validated.
8	Invasion and epithelial-mesenchymal transition	MMP2 ↓; MMP9 ↓; Wnt/β-catenin ↓; EMT ↓; migration ↓; invasion ↓	↔ or epithelial barrier integrity ↑	G	Anti-invasive phenotype	Often secondary to NF-κB, AKT, MAPK, and Wnt pathway modulation.
9	NRF2 antioxidant response	NRF2 ↑ or ↓ (context-dependent); HO-1 ↑ or ↓; redox adaptation altered	NRF2 ↑; HO-1 ↑; GSH ↑; SOD ↑; catalase ↑	R, G	Secondary redox adaptation	NRF2 activation is generally cytoprotective in normal tissue but may protect some cancers; prostate-cancer findings indicate model-dependent alteration of the NRF2 HO-1 BACH1 axis.
10	Glycolysis and lipid metabolism	LDH activity ↓; lactate production ↓; FASN ↓; glycolytic dependence ↓ (model-dependent)	↔	R, G	Metabolic growth restriction	The evidence base is smaller and less consistent than that for redox modulation and apoptosis; avoid treating glycolysis inhibition as universal.
11	DNA damage and repair balance	DNA damage ↑; p53 response ↑; FEN1 ↓ in nanoparticle studies; repair capacity ↓ (model-dependent)	Oxidative DNA damage ↓ at antioxidant exposure	R, G	Genotoxic stress in cancer cells	Free GA and GA-containing nanocarriers are not mechanistically interchangeable; nanoparticle-specific findings require separate qualification.
12	Chemosensitization	Paclitaxel response ↑; carboplatin response ↑; camptothecin response ↑; olaparib response ↑ (model-dependent)	Chemotherapy-associated injury ↓ or ↔ in limited models	G	Adjunctive treatment sensitization	Evidence is primarily in vitro. Both antioxidant protection and pro-oxidant sensitization are possible, making unsupervised clinical combinations inappropriate.
13	Immune checkpoint and tumor immunity	PD-L1 ↓; CD8-positive T-cell activity ↑; antitumor immune response ↑ (model-dependent)	Immune homeostasis modulation ↔	G	Immune sensitization	Promising animal evidence exists, but direct clinical immunotherapy enhancement has not been demonstrated.
14	Clinical Translation Constraint	Free systemic GA exposure ↓; conjugation ↑; metabolism ↑; cytotoxic target exposure often not reached	Dietary exposure generally tolerated; high-dose isolated exposure insufficiently characterized	R, G	Exposure and evidence limitation	Rapid metabolism, uncertain tumor delivery, formulation heterogeneity, high in-vitro concentrations, and absence of isolated-GA cancer trials limit translation.

P: 0–30 min R: 30 min–3 hr G: >3 hr

ROS, Reactive Oxygen Species: Click to Expand ⟱

Source: HalifaxProj (inhibit)

Type:

Reactive oxygen species (ROS) are highly reactive molecules that contain oxygen and can lead to oxidative stress in cells. They play a dual role in cancer biology, acting as both promoters and suppressors of cancer.
ROS can cause oxidative damage to DNA, leading to mutations that may contribute to cancer initiation and progression. So normally you want to inhibit ROS to prevent cell mutations.
However excessive ROS can induce apoptosis (programmed cell death) in cancer cells, potentially limiting tumor growth. Chemotherapy typically raises ROS.
-mitochondria is the main source of reactive oxygen species (ROS) (and the ETC is heavily related)
ROS Homeostasis in Cancer Cells and Its Potential as a Therapeutic Target

"Reactive oxygen species (ROS) are two electron reduction products of oxygen, including superoxide anion, hydrogen peroxide, hydroxyl radical, lipid peroxides, protein peroxides and peroxides formed in nucleic acids 1. They are maintained in a dynamic balance by a series of reduction-oxidation (redox) reactions in biological systems and act as signaling molecules to drive cellular regulatory pathways."
"During different stages of cancer formation, abnormal ROS levels play paradoxical roles in cell growth and death 8. A physiological concentration of ROS that maintained in equilibrium is necessary for normal cell survival. Ectopic ROS accumulation promotes cell proliferation and consequently induces malignant transformation of normal cells by initiating pathological conversion of physiological signaling networks. Excessive ROS levels lead to cell death by damaging cellular components, including proteins, lipid bilayers, and chromosomes. Therefore, both scavenging abnormally elevated ROS to prevent early neoplasia and facilitating ROS production to specifically kill cancer cells are promising anticancer therapeutic strategies, in spite of their contradictoriness and complexity."
"ROS are the collection of derivatives of molecular oxygen that occur in biology, which can be categorized into two types, free radicals and non-radical species. The non-radical species are hydrogen peroxide (H 2O 2 ), organic hydroperoxides (ROOH), singlet molecular oxygen ( 1 O 2 ), electronically excited carbonyl, ozone (O3 ), hypochlorous acid (HOCl, and hypobromous acid HOBr). Free radical species are super-oxide anion radical (O 2•−), hydroxyl radical (•OH), peroxyl radical (ROO•) and alkoxyl radical (RO•) [130]. Any imbalance of ROS can lead to adverse effects. H2 O 2 and O 2 •− are the main redox signalling agents. The cellular concentration of H2 O 2 is about 10−8 M, which is almost a thousand times more than that of O2 •−".
"Radicals are molecules with an odd number of electrons in the outer shell [393,394]. A pair of radicals can be formed by breaking a chemical bond or electron transfer between two molecules."

Recent investigations have documented that polyphenols with good antioxidant activity may exhibit pro-oxidant activity in the presence of copper ions, which can induce apoptosis in various cancer cell lines but not in normal cells. "We have shown that such cell growth inhibition by polyphenols in cancer cells is reversed by copper-specific sequestering agent neocuproine to a significant extent whereas iron and zinc chelators are relatively ineffective, thus confirming the role of endogenous copper in the cytotoxic action of polyphenols against cancer cells. Therefore, this mechanism of mobilization of endogenous copper." > Ions could be one of the important mechanisms for the cytotoxic action of plant polyphenols against cancer cells and is possibly a common mechanism for all plant polyphenols. In fact, similar results obtained with four different polyphenolic compounds in this study, namely apigenin, luteolin, EGCG, and resveratrol, strengthen this idea.
Interestingly, the normal breast epithelial MCF10A cells have earlier been shown to possess no detectable copper as opposed to breast cancer cells [24], which may explain their resistance to polyphenols apigenin- and luteolin-induced growth inhibition as observed here (Fig. 1). We have earlier proposed [25] that this preferential cytotoxicity of plant polyphenols toward cancer cells is explained by the observation made several years earlier, which showed that copper levels in cancer cells are significantly elevated in various malignancies. Thus, because of higher intracellular copper levels in cancer cells, it may be predicted that the cytotoxic concentrations of polyphenols required would be lower in these cells as compared to normal cells."

Majority of ROS are produced as a by-product of oxidative phosphorylation, high levels of ROS are detected in almost all cancers.
-It is well established that during ER stress, cytosolic calcium released from the ER is taken up by the mitochondrion to stimulate ROS overgeneration and the release of cytochrome c, both of which lead to apoptosis.

Note: Products that may raise ROS can be found using this database, by:
Filtering on the target of ROS, and selecting the Effect Direction of ↑

Targets to raise ROS (to kill cancer cells):
• NADPH oxidases (NOX): NOX enzymes are involved in the production of ROS.
    -Targeting NOX enzymes can increase ROS levels and induce cancer cell death.
    -eNOX2 inhibition leads to a high NADH/NAD⁺ ratio which can lead to increased ROS
• Mitochondrial complex I: Inhibiting can increase ROS production
• P53: Activating p53 can increase ROS levels(by inducing the expression of pro-oxidant genes)
• Nrf2 inhibition: regulates the expression of antioxidant genes. Inhibiting Nrf2 can increase ROS levels
• Glutathione (GSH): an antioxidant. Depleting GSH can increase ROS levels
• Catalase: Catalase converts H2O2 into H2O+O. Inhibiting catalase can increase ROS levels
• SOD1: converts superoxide into hydrogen peroxide. Inhibiting SOD1 can increase ROS levels
• PI3K/AKT pathway: regulates cell survival and metabolism. Inhibiting can increase ROS levels
• HIF-1α inhibition: regulates genes involved in metabolism and angiogenesis. Inhibiting HIF-1α can increase ROS
• Glycolysis: Inhibiting glycolysis can increase ROS levels • Fatty acid oxidation: Cancer cells often rely on fatty acid oxidation for energy production.
-Inhibiting fatty acid oxidation can increase ROS levels
• ER stress: Endoplasmic reticulum (ER) stress can increase ROS levels
• Autophagy: process by which cells recycle damaged organelles and proteins.
-Inhibiting autophagy can increase ROS levels and induce cancer cell death.
• KEAP1/Nrf2 pathway: regulates the expression of antioxidant genes.
    -Inhibiting KEAP1 or activating Nrf2 can increase ROS levels and induce cancer cell death.
• DJ-1: regulates the expression of antioxidant genes. Inhibiting DJ-1 can increase ROS levels
• PARK2: regulates the expression of antioxidant genes. Inhibiting PARK2 can increase ROS levels
• SIRT1 inhibition:regulates the expression of antioxidant genes. Inhibiting SIRT1 can increase ROS levels
• AMPK activation: regulates energy metabolism and can increase ROS levels when activated.
• mTOR inhibition: regulates cell growth and metabolism. Inhibiting mTOR can increase ROS levels
• HSP90 inhibition: regulates protein folding and can increase ROS levels when inhibited.
• Proteasome: degrades damaged proteins. Inhibiting the proteasome can increase ROS levels
• Lipid peroxidation: a process by which lipids are oxidized, leading to the production of ROS.
    -Increasing lipid peroxidation can increase ROS levels
• Ferroptosis: form of cell death that is regulated by iron and lipid peroxidation.
    -Increasing ferroptosis can increase ROS levels
• Mitochondrial permeability transition pore (mPTP): regulates mitochondrial permeability.
    -Opening the mPTP can increase ROS levels
• BCL-2 family proteins: regulate apoptosis and can increase ROS levels when inhibited.
• Caspase-independent cell death: a form of cell death that is regulated by ROS.
    -Increasing caspase-independent cell death can increase ROS levels
• DNA damage response: regulates the repair of DNA damage. Increasing DNA damage can increase ROS
• Epigenetic regulation: process by which gene expression is regulated.
    -Increasing epigenetic regulation can increase ROS levels

-PKM2, but not PKM1, can be inhibited by direct oxidation of cysteine 358 as an adaptive response to increased intracellular reactive oxygen species (ROS)

ProOxidant Strategy:(inhibit the Mevalonate Pathway (likely will also inhibit GPx)
-HydroxyCitrate (HCA) found as supplement online and typically used in a dose of about 1.5g/day or more
-Atorvastatin typically 40-80mg/day, -Dipyridamole typically 200mg 2x/day Combined effect research
-Lycopene typically 100mg/day range (note debatable as it mainly lowers NRF2)

Dual Role of Reactive Oxygen Species and their Application in Cancer Therapy

ROS-Inducing Interventions in Cancer — Canonical + Mechanistic Reference
-generated from AI and Cancer database
ROS rating:  +++ strong | ++ moderate | + weak | ± mixed | 0 none
NRF2:        ↓ suppressed | ↑ activated | ± mixed | 0 none
Conditions:  [D] dose  [Fe] metal  [M] metabolic  [O₂] oxygen
             [L] light [F] formulation [T] tumor-type [C] combination


Item  ROS↑  NRF2  Condition  Mechanism Class  Remarks  

ROS">Piperlongumine
+++  ↓  [D][T]  ROS-dominant
Selective <span class="wphighlight">ROS</span> stressor, Prevents compensatory upregulation of NRF2, ie GSH↓



ROS">Shikonin
+++ ↓/± [D][T] ROS-dominant
<span class="wphighlight">ROS</span> + glycolysis + GPX4 inhibition



ROS">Vitamin K3 (menadione)
+++ ↓ [D] ROS-dominant
Quinone redox cycler; toxicity limits use



ROS">Copper (ionic / nano)
+++ ↓ [Fe][F] ROS-dominant
Fenton-type redox chemistry



ROS">Sodium Selenite
+++ ↓ [D] ROS-dominant
Pro-oxidant, depletes GSH



ROS">Juglone
+++ ↓ [D] ROS-dominant
Strong quinone <span class="wphighlight">ROS</span> chemistry



ROS">Auranofin
+++ ↓ [D] ROS-dominant
TrxR inhibition → redox collapse



ROS">Photodynamic Therapy (PDT)
+++ 0 [L][O₂] ROS-dominant
Singlet oxygen is core cytotoxic mechanism



ROS">Radiotherapy / Radiation
+++ 0 [O₂] ROS-dominant
DNA damage largely via <span class="wphighlight">ROS</span>



ROS">Doxorubicin
+++ ↓ [D] ROS-dominant
Chemo; redox cycling + mitochondrial <span class="wphighlight">ROS</span>



ROS">Cisplatin
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span> contributes to DNA/protein damage



ROS">Salinomycin
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span>-mediated CSC toxicity



ROS">Artemisinin / DHA
++ ↓ [Fe][T] ROS-dominant
Iron-activated radical generation



ROS">Sulfasalazine
++ ↓ [C][T] ROS-dominant
Ferroptosis; xCT inhibition → lipid <span class="wphighlight">ROS</span>



ROS">FMD / fasting
++ ↓ [M][C][O₂] ROS-dominant
Metabolic stress → mitochondrial <span class="wphighlight">ROS</span>



ROS">Vitamin C (pharmacologic)
++ ↓ [Fe][D] ROS-dominant
Extracellular H₂O₂ at high dose



ROS">Silver nanoparticles
++ ± [F][D] ROS-dominant
<span class="wphighlight">ROS</span> common; selectivity unreliable



ROS">Gambogic acid
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span>-mediated apoptosis



ROS">Parthenolide
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span> + NF-κB suppression



ROS">Plumbagin
++ ↓ [D] ROS-dominant
Quinone <span class="wphighlight">ROS</span> driver



ROS">Allicin
++ ↓ [D] ROS-dominant
Thiol-reactive oxidative stress



ROS">Ashwagandha (Withaferin A)
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span>-mediated apoptosis



ROS">Berberine
++ ↓ [D][M] ROS-dominant
Mitochondrial <span class="wphighlight">ROS</span> induction



ROS">PEITC
++ ↓ [D][C] ROS-dominant
GSH depletion + <span class="wphighlight">ROS</span>



ROS">Methionine restriction
+ ↓ [M][C][T] ROS-secondary
Redox vulnerability increased; <span class="wphighlight">ROS</span> indirect



ROS">DCA
+ ± [M][T] ROS-secondary
<span class="wphighlight">ROS</span> via forced OXPHOS



ROS">Capsaicin
+ ± [D][T] ROS-secondary
Ca²⁺ stress → <span class="wphighlight">ROS</span>



ROS">Galloflavin
+ 0 [D] ROS-secondary
<span class="wphighlight">ROS</span> not primary driver



ROS">Piperine
+ ± [D][F] ROS-secondary
Weak <span class="wphighlight">ROS</span> induction



ROS">Propyl gallate
+ ↓ [D] ROS-secondary
Pro-oxidant at high dose



ROS">Scoulerine
+ ? [D][T] ROS-secondary
Sparse <span class="wphighlight">ROS</span> data



ROS">Thymoquinone
± ± [D][T] Dual redox
Antioxidant ↔ pro-oxidant switch



ROS">Emodin
± ± [D][T] Dual redox
Not cancer-exclusive



ROS">Alpha-lipoic acid (ALA)
± ↑ [D][M] NRF2-dominant
Antioxidant at low dose



ROS">Curcumin
± ↑/↓ [D][F] NRF2-dominant
Hormetic redox behavior



ROS">EGCG
± ↑/↓ [D][O₂] NRF2-dominant
Auto-oxidation artifacts common



ROS">Quercetin
± ↑/↓ [D][Fe] NRF2-dominant
GSH-dependent cycling



ROS">Resveratrol
± ↑ [D][M] NRF2-dominant
<span class="wphighlight">ROS</span> only at high dose



ROS">Sulforaphane
± ↑↑ [D] NRF2-dominant
Strong NRF2 activator



ROS">Lycopene
0 ↑ — Antioxidant
Consistently antioxidant



ROS">Rosmarinic acid
0 ↑ — Antioxidant
Primarily antioxidant



ROS">Citrate
0 0 — Neutral
Metabolic; not a <span class="wphighlight">ROS</span> agent

Scientific Papers found: Click to Expand⟱

7032-

GA,

Cisplatin,

Gallic acid: a polyphenolic compound potentiates the therapeutic efficacy of cisplatin in human breast cancer cells

in-vitro,

BC,

MCF7

in-vitro,

Nor,

MCF10

ChemoSen↑, tumCV↓, Apoptosis↑, selectivity↑, *ROS↓, eff↑, *chemoP↑, Dose↝,

7049-

GA,

Pharmacological effects of gallic acid in health and diseases: A mechanistic review

Review,

Var,

*antiOx↑, *Inflam↓, *antiNeop↑, *cardioP↑, *Bacteria↓, *AST↓, *ALAT↓, *ALP↓, *lipid-P↓, *GSH↑, *Catalase↑, *GPx↑, *GSTs↑, *Urea↓, *creat↓, tumCV↓, TumCCA↑, i-Ca+2↑, CDK1↑, Casp3↑, Casp8↑, Casp9↑, MMP↓, ROS↑, MMPs↓, *GastroP↑, *hepatoP↑, *ROS↓, *AChE↑,

7035-

GA,

Gallic acid attenuates LPS-induced inflammation in Caco-2 cells by suppressing the activation of the NF-κB/MAPK signaling pathway

in-vitro,

IBD,

Caco-2

*Inflam↓, *antiOx↑, *CLDN1↓, *OCLN↓, *ZO-1↓, *IL6↓, *IL1β↓, *TNF-α↓, *BAX↓, *BAD↓, *Casp3↓, *Casp8↓, *ROS↓, *SOD↑, *Catalase↑, *GSH↑, *TJ↑, *Apoptosis↓, *NF-kB↓, *MAPK↓,

7034-

GA,

RES,

The Growth Inhibitory Effect of Resveratrol and Gallic Acid on Prostate Cancer Cell Lines through the Alteration of Oxidative Stress Balance: The Interplay between Nrf2, HO-1, and BACH1 Genes

in-vitro,

Pca,

PC3

in-vitro,

Pca,

DU145

TumCG↓, ROS↓, SOD↑, GPx↑, Catalase↑, GSR↑, GSH↑, HO-1↑, NRF2↑,

7033-

GA,

OL,

Gallic Acid Enhances Olaparib-Induced Cell Death and Attenuates Olaparib Resistance in Human Osteosarcoma U2OS Cell Line

in-vitro,

OS,

U2OS

tumCV↓, angioG↓, DNAdam↑, Apoptosis↑, cl‑PARP↓, Bcl-2↓, BAX↑, ROS↓, eff↑, TumCMig↓, VEGF↓, Casp9↑, P53↑, selectivity↑,

7029-

GA,

Gallic acid induces G1 phase arrest and apoptosis of triple-negative breast cancer cell MDA-MB-231 via p38 mitogen-activated protein kinase/p21/p27 axis

in-vitro,

BC,

MDA-MB-231

in-vitro,

BC,

HS587T

in-vitro,

Nor,

MCF10

AntiTum↑, tumCV↓, selectivity↑, TumCCA↑, cycD1/CCND1↓, CDK4↓, cycE/CCNE↓, CDK2↓, P21↑, p27↑, Casp9↑, Casp3↑, ROS↑, mtDam↑, i-Ca+2↑, *ROS↓, *Apoptosis↓, TumCG↓,

7036-

TBE,

GA,

Terminalia bellirica (Gaertn.) Roxb. Extract and Gallic Acid Attenuate LPS-Induced Inflammation and Oxidative Stress via MAPK/NF-κB and Akt/AMPK/Nrf2 Pathways

in-vitro,

Nor,

THP1

in-vitro,

Nor,

RAW264.7

*ROS↓, *MAPK↓, *NF-kB↓, *TAC↑, *NRF2↑, *Akt↑, *AMPK↑, *Inflam↓,

Showing Research Papers: 1 to 7 of 7

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 7

Pathway results for Effect on Cancer / Diseased Cells:

Functional Outcomes(tgid=23) ⓘ

AntiTum↑, 1,
Total Targets: 40

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 2, Catalase↑, 2, GPx↑, 1, GSH↑, 2, GSTs↑, 1, lipid-P↓, 1, NRF2↑, 1, ROS↓, 5, SOD↑, 1, TAC↑, 1,

Core Metabolism/Glycolysis(tgid=4) ⓘ

ALAT↓, 1, AMPK↑, 1,

Cell Death(tgid=5) ⓘ

Akt↑, 1, Apoptosis↓, 2, BAD↓, 1, BAX↓, 1, Casp3↓, 1, Casp8↓, 1, MAPK↓, 2,

Migration(tgid=13) ⓘ

CLDN1↓, 1, TJ↑, 1, ZO-1↓, 1,

Barriers & Transport(tgid=15) ⓘ

GastroP↑, 1, OCLN↓, 1,

Immune & Inflammatory Signaling(tgid=16) ⓘ

IL1β↓, 1, IL6↓, 1, Inflam↓, 3, NF-kB↓, 2, TNF-α↓, 1,

Synaptic & Neurotransmission(tgid=18) ⓘ

AChE↑, 1,

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 1, ALP↓, 1, AST↓, 1, creat↓, 1, IL6↓, 1, Urea↓, 1,

Functional Outcomes(tgid=23) ⓘ

antiNeop↑, 1, cardioP↑, 1, chemoP↑, 1, hepatoP↑, 1,

Infection & Microbiome(tgid=24) ⓘ

Bacteria↓, 1,
Total Targets: 41

Scientific Paper Hit Count for: ROS, Reactive Oxygen Species

7 Gallic acid
1 Cisplatin
1 Resveratrol
1 olaparib/LYNPARZA
1 Terminalia bellirica

Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:82  Target#:275  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

Gallic acid / ROS Cancer Research Results

Gallic Acid Mechanistic Profile

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress(tgid=1) ⓘ

Mitochondria & Bioenergetics(tgid=3) ⓘ

Cell Death(tgid=5) ⓘ

Transcription & Epigenetics(tgid=7) ⓘ

DNA Damage & Repair(tgid=10) ⓘ

Cell Cycle & Senescence(tgid=11) ⓘ

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

Migration(tgid=13) ⓘ

Angiogenesis & Vasculature(tgid=14) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Functional Outcomes(tgid=23) ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress(tgid=1) ⓘ

Core Metabolism/Glycolysis(tgid=4) ⓘ

Cell Death(tgid=5) ⓘ

Migration(tgid=13) ⓘ

Barriers & Transport(tgid=15) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Synaptic & Neurotransmission(tgid=18) ⓘ

Clinical Biomarkers(tgid=22) ⓘ

Functional Outcomes(tgid=23) ⓘ

Infection & Microbiome(tgid=24) ⓘ

Home Page